The low-metastatic RSV-transformed fibrosarcoma line B77-3T3 and its metastatic variant AA12, selected in vitro, have been analysed by blot and in situ hybridization with v-src and murine c-myc specific probes in order to detect molecular rearrangements underlying the transition from the low-metastatic to the high-metastatic phenotype. Previous cytogenetic analysis had evidenced that a marker chromosome of the parental tumor line (chromosome A) is replaced in the metastatic counterpart by a new marker chromosome (chromosome B), possibly arisen by duplication of a chromosome A segment, included between two C-positive regions (L. Doneda et al., 1985). In situ hybridization on chromosome spreads of the two related lines with a (3)H-labelled v-src probe showed that src sequences are located within the marker chromosomes A and B, and the percentage of grains over the AA12 marker chromosome is always double that found on the B77-3T3 marker. These signals were considered to identify v-src sequences as they were found to be slightly amplified in the metastatic variant DNA by blot hybridization with the v-src probe. As regards the intrachromosomal location of the signals, most grains were clustered near the heterochromatic bands, suggesting a possible role for heterochromatic sites in tumor formation and evolution. No involvement of the A and B marker chromosomes was shown by in situ hybridization experiments with a c-myc probe. However the dosage of c-myc sequences was also found to be slightly increased in the metastatic variant DNA.

Localization of viral transforming sequences within marker chromosomes associated with tumor formation and progression in a murine fibrosarcoma / L. Doneda, P. Custode, C. De Giuli Moreghen, L. Larizza. - In: CYTOTECHNOLOGY. - ISSN 0920-9069. - 1:1(1988), pp. 47-55.

Localization of viral transforming sequences within marker chromosomes associated with tumor formation and progression in a murine fibrosarcoma

L. Doneda
Primo
;
C. De Giuli Moreghen;L. Larizza
Ultimo
1988

Abstract

The low-metastatic RSV-transformed fibrosarcoma line B77-3T3 and its metastatic variant AA12, selected in vitro, have been analysed by blot and in situ hybridization with v-src and murine c-myc specific probes in order to detect molecular rearrangements underlying the transition from the low-metastatic to the high-metastatic phenotype. Previous cytogenetic analysis had evidenced that a marker chromosome of the parental tumor line (chromosome A) is replaced in the metastatic counterpart by a new marker chromosome (chromosome B), possibly arisen by duplication of a chromosome A segment, included between two C-positive regions (L. Doneda et al., 1985). In situ hybridization on chromosome spreads of the two related lines with a (3)H-labelled v-src probe showed that src sequences are located within the marker chromosomes A and B, and the percentage of grains over the AA12 marker chromosome is always double that found on the B77-3T3 marker. These signals were considered to identify v-src sequences as they were found to be slightly amplified in the metastatic variant DNA by blot hybridization with the v-src probe. As regards the intrachromosomal location of the signals, most grains were clustered near the heterochromatic bands, suggesting a possible role for heterochromatic sites in tumor formation and evolution. No involvement of the A and B marker chromosomes was shown by in situ hybridization experiments with a c-myc probe. However the dosage of c-myc sequences was also found to be slightly increased in the metastatic variant DNA.
C-heterochromatin; marker chromosomes; tumor progression; v-src sequences
Settore MED/03 - Genetica Medica
Settore BIO/13 - Biologia Applicata
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/2434/188665
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